ArticleNature communications2025
Remodeling adipocytes' lipid metabolism with a polycation loaded enzyme-active framework reverses osteoporotic bone marrow.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Beyond M1/M2: The Pivotal Role of Macrophage Metabolic Reprogramming in Chronic Bone Disease and Targeted Intervention.International journal of molecular sciences · 2026Review
- Pearl-Like Bioinspired Coating Enables Regulation of Mg Degradation for Osteoporotic Bone Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Antioxidant Nanozymes: From Rational Design to Biomedical Applications.Research (Washington, D.C.) · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
The function of osteoporosis-induced bone marrow adipocyte (BMAds) accumulation remains inadequately understood. Here, we analyze bone marrow lipidomic data and reveal that BMAds deteriorate the skeletal microenvironment by secreting large amounts of lipids, altering the senescence status of neighboring cells by affecting their mitochondrial function. To specifically target BMAds under osteoporotic conditions, we design a polycation-loaded biomimetic dual-site framework (CZP@LC) that interferes with lipid crosstalk between BMAds and neighboring bone marrow cells. Shutting down abnormal lipid metabolism and secretion in adipocytes mitigates mitochondrial dysfunction in neighboring cells, which prevents bone marrow cells from senescing. The inhibition of lipid synthesis in BMAds blocks bone marrow stromal cells from differentiating into adipocytes, interrupting the vicious cycle. Moreover, interruption of lipid communication rescues osteoblasts from mitochondrial dysfunction-induced senescence and restores osteogenesis. Here we demonstrate the metabolic mechanisms of BMAds and lipid crosstalk in osteoporosis, provide a potential avenue for targeted biotherapy.
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Registered trials
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